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HyperK and Shades of Grey: Myths and Facts about Hyperkalemia Part II

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Today we continue our discussion about the myths and facts of hyperkalemia with Dr. Brooks Walsh, author of the Mill Hill Ave Command blog. We also feature contributions from Dr. Stephen Smith, of Dr. Smith's ECG Blog.

If you would like to refresh your memory on Part I visit here.                                         

Dr. Walsh and I spoke about why he thought hyperkalemia presented such a challenge for EMS providers:

"The recognition and treatment of hyperkalemia is one of those areas in medicine where, despite strong and clinically relevant results in the literature, the "usual practice" keeps kicking along. This is like a lot of areas in medicine, true."

With that said, let us continue with Myths and Facts about Hyperkalemia Part II:

 

Myth: The ECG shows a predictable sequence of changes as the potassium level increases

Experiments done on (presumably) healthy animals demonstrated a progression in ECG derangements as potassium levels were experimentally raised. A number of textbooks and review articles repeat this result, even though numerous human clinical studies have failed to replicate a linear relationship between the potassium level and specific ECG findings.

For example, one review article, much referenced in the EM literature, presents a table describing the correlations between potassium levels and expected ECG findings.

 

But the literature is full of case report that argue against such tidy correlations: here's a case of a woman with a potassium of almost 8, and complete AV block  but no QRS widening or T-wave tenting; here is a similar case with a K of 7.5; we even see that a patient can develop an AV block with a K level of just 5.5! On the other hand, here's a case of complete AV block with a narrow QRS, but a potassium of just 6.4.

We asked Dr. Stephen Smith about his experiences with this issue. He agreed and said he has seen patients go into VF after having only peaked T waves. You can see examples of this here.

So it seems better to avoid thinking that you can determine a specific potassium range on the ECG, but rather that it can suggest a generally elevated level. Any of the "expected ECG abnormalities" can occur at any level of potassium.

 

 

Myth: Calcium is a dangerous medication

Make no mistake – IV calcium can be a potent drug, but with potential benefits. And you should always refer to your local guidelines/protocols for the last word on when you can & should give it.  

But that being said, there is some concern voiced by clinicians about administering "one mustard box." Let's talk about 2 big concerns that people seem to have with giving calcium: skin necrosis and digoxin toxicity.

So, how worried should you be about skin necrosis? EMS usually carries calcium chloride, which has some potential to cause problems if it extravasates (calcium gluconate has a lower risk, and can be given subcutaneously for some problems). As a result, many people have a lot of concern about administering the medication, fearing the risks if the IV leaks or fails. 

Well, yes, you must assure yourself that you have a patent, free-lowing line in a big vein! But on the other hand, you have already been taking risks with injecting dextrose 50% and sodium bicarbonate, as both are known to cause skin necrosis. 

For example:

 

 Ann Emerg Med. 2006;48:236

This patient came into the ED with hyperkalemia, and was treated with IV insulin and dextrose (no calcium). 

Or how about this hand?

 

Ann. Surg. – November 1975

That's a neonate who was getting a D10% drip in his hand.

There are a small number of case reports of bad calcium extravasations, but that rare risk must be balanced against the immediate, and unpredictable, risk of life-threatening arrhythmias.

Some EMS-toxicologists may also point to the historical concern with digoxin toxicity, that calcium infusions could provoke a "stone heart," or cardiac tetany. A recent pig study had cast a lot of doubt on that thinking. And then a retrospective study was published in 2012 by Levine et al., which looked at patients with digoxin toxicity, some of whom were also treated with calcium. They found no effect on mortality – no "stone heart ' – and another myth was dispelled.

 

 

So you should feel comfortable giving calcium when you think you're dealing with hyperkalemia. But don't just take my word for it – listen to some medical experts!  

For example, from a nephrology paper:  

 "When uncertain of the importance of a raised potassium level, it is prudent to go ahead and administer calcium gluconate, as the downside risk is minimal."    Aslam 2002

Again, ECG master Stephen Smith:

"[G]iven the fact that calcium therapy is benign… when I suspect hyperkalemia I just given calcium immediately, even before I get the potassium back. … There are so many ways the ECG can manifest with severe hyperkalemia — life-threatening hyperkalemia. Again, the treatment is benign, and cheap! So how many life-threatening diseases can you treat benignly and cheaply?"

You can hear Dr. Smith expand on this by listening to him on  EMCRIT podcast 42.

 

 

Practical point: How to give albuterol for hyperkalemia

Albuterol may in fact have a role in the prehospital treatment of hyperkalemia. It works by shifting potassium from the serum into the cells.

Consider this case study abstract:

"Growing evidence suggests that there may be a role for albuterol in the treatment of patients with severe hyperkalemia…β2 agonist administration was found to be safe and was associated with a significant decrease in serum potassium levels. Therefore, β2 agonist therapy should be considered as an adjunctive treatment for patients with severe hyperkalemia."

Or this:

"In the doses used, nebulized albuterol therapy resulted in a prompt and significant decrease in the plasma potassium concentrations in patients on hemodialysis, and caused no adverse cardiovascular effects (Allon).

You can use an albuterol in a nebulizer, or can use levalbuterol if that's what you have (Pancu). And it doesn't have to be a neb – it can also be an MDI with a spacer (Mandelberg).

But how much to we give? Of the medics who are savvy enough to want to use Albuterol to treat hyperkalemia, few of them know the effective dose needed to treat.

You can give 5mg (McClure), 10, or even 20mg (Allon), if you are using a nebulizer. The dose of 10-20 mg seems to be the dose most often used. 

Perhaps you realize that the "standard dose" we use to treat bronchoconstriction is 2.5mg/3ml. It is problematic to consider loading at least 4 doses into a small volume nebulizer. That's not really going to work. 

Albuterol does come prepared as 2.5 mg/0.5ml. Now we are talking about 2 ml's, which is much easier to manage and a better choice for treating hyperkalemia.

Is it worth stocking multiple doses of Albuterol? Perhaps. It is not going to be the first line treatment for hyperkalemia, so the decision will vary by system. Needless to say, if you are going to treat with Albuterol, make sure you have an effective way to do it.

 

We hope you have enjoyed this short series on the Myths and Facts about Hyperkalemia. 

My thanks again to Dr. Brooks Walsh, as well as Dr. Stephen Smith for their valued contributions.

As usual, all comments and opinions are encouraged!

Posted by on January 14, 2013 • Filed under: ems-health-safety, ems-topics, patient-management, Training, training-development • Tagged: , , , , , , ,

HyperK and Shades of Grey: Myths and Facts about Hyperkalemia Part I

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Happy New Year everybody!

We start 2013 with a continuation of our discussion about the field treatment of hyperkalemia. 

It might be helpful to review the first part of the discussion," HyperK and Shades of Grey" here. 

We are fortunate to have as a guest contributor Dr. Brooks Walsh of the Mill Hill Ave Command blog. An advocate of prehospital medicine, Dr. Walsh offers shares "Myths and Facts" of hyperkalemia with us. My sincerest thanks him for his valued contributions! 

I asked Dr. Walsh why he thought hyperkalemia presented such a challenge for EMS providers. Here is what he had to say:

"The recognition and treatment of hyperkalemia is one of those areas in medicine where, despite strong & clinically relevant results in the literature, the "usual practice" keeps kicking along. This is like a lot of areas in medicine, true.

But rather than curse the darkness, I wanted to go over some newer perspectives on hyperkalemia. Now, I don't want to simply reiterate all the great material that Dr. Weingart talked about on EMCRIT, so you really ought to download his great podcasts on the treatment of hyperkalemia and on why Kayexalate is likely ineffective, if not outright dangerous. The podcasts are real short, so just play them right now.

With that said, I'd like to review a few topics in hyperkalemia that deserve more attention:

 

Myth: Dialysis patients tolerate hyperkalemia better than other people.

Medicine is funny. I mean, there are "facts" that "everyone knows," but that are surprisingly hard to prove in studies. This is sort of one of those kind of facts, with very little evidence, and plenty of "real world" experience. Should we continue to believe it?

Maybe. It kind of depends on what we mean by "tolerate." If we mean "don't show ECG signs of hyperkalemia," then maybe dialysis patients do "tolerate" hyperkalemia better than other people. 

It's kind of hard to answer this definitively, though, since ECG signs of hyperkalemia, especially in the moderate range (e.g. < 6.5), are often absent on the ECG on all patients. We just don't see that many patients, dialysis or no, with severe hyperkalemia. Even in a study that looked only at dialysis patients, the vast majority had a K < 5.2, and ECG changes were accordingly infrequent.

But it may also be that dialysis patients, in fact, do show fewer signs of hyperkalemia on the ECG than do other people. A study done back in 1967 looked at dogs that received IV potassium slowly or quickly (but ending up at the same blood level). The faster infusions caused more ECG and hemodynamic effects. It is possible that ESRD patients, with a presumably slow increase in potassium levels, show fewer ECG changes than, say, a patient with acute rhabdomyolysis.

But the ability to avoid ECG changes isn't the "tolerance" we care about in hyperkalemia - we really care about the potential for patients to go into cardiac arrest. Hyperkalemia, regardless of ECG signs, puts the patient at risk for fatal arrhythmias. If you have either lab results or ECG evidence of hyperkalemia, that patient needs to be treated immediately – on that, most experts agree. I couldn't find any mention in the literature that suggests otherwise. For example:

                   "We emphasize that despite the absence of ECG changes of hyperkalaemia in ESRD, hyperkalaemia is still a     potentially life-threatening condition." –Aslam 2002

Or

"Some experts advocate calcium administration in patients whose serum potassium is >6.0–6.5 mm, even in the absence of EKG changes." –Putcha 2007 

 

Myth: If the ECG doesn't show QRS widening, then the patient is at low risk.

Some clinicians are under the impression that you can wait to treat the hyperkalemia until the QRS is "incredibly widened," showing huge sine-waves.  An ECG that shows "just T-waves" is presumably at lower risk, in this view.

Except that's not how it works, according to the experts. As these nephrologists explain:

                 "Five medical textbooks (two nephrology, two internal medicine, and one emergency medicine) advocate calcium gluconate in all hyperkalemic patients with EKG changes. "

Or this critical-care nephrologist:

                "It is apparent that neither the EKG nor the [potassium level] alone is an adequate index of the urgency of hyperkalemia,… hyperkalemia should be treated emergently for 1) K > 6.5 mmol/L or 2) EKG manifestations of hyperkalemia regardless of the [level]." –Weisberg 2008 "Management of severe hyperkalemia"

We asked Dr. Smith about his experiences with this topic, whether he has seen patients arrest without going through the ECG transition to widened, sine wave ECGs. His response as well was that "I have seen v-fib with peaked T waves only" on the ECG.

Stay tuned for "Myths and Facts Part II"!

 

Posted by on December 31, 2012 • Filed under: ems-health-safety, ems-topics, patient-management, Training, training-development • Tagged: , , , , , , ,

63 year old male CC: Substernal Chest Pain – Discussion

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This is the discussion for 63 year old male CC: Substernal Chest Pain, brought to you by Dr. Brooks Walsh of Mill Hill Avenue Command and Doc Cottle's Desk. Be sure to review the first part!

When we last left off, our patient was a 63 year old male complaining of substernal chest pain which awoke him from sleep. We obtained standard, right-sided, and posterior ECG's which cardiology deemed non-specific. Our patient continued to have persistent chest pain even after maximal therapy.

Coronary catheterization was performed later that morning, and a total occlusion of the first obtuse marginal (OM1), a branch of the circumflex artery, was found. A drug eluting stent was placed, and his subsequent hospital course was unremarkable.

Could we have guessed this from the start? Let's take a look at his ECG's again:

I Think Your Segments are Upside Down - Initial 12-Lead

Reviewing our patient's first ECG we see horizontal ST segment depression of 1 mm was seen in II and aVF, 3 mm ST depression in V2, and 1 mm ST depression in V3 and V4, all with upright T waves. An early R-wave transition was noted, with a height of 13 mV and an R/S of 1 in V2. Lead III showed T wave inversion.

I Think Your Segments are Upside Down - Right-Sided 12-Lead

The right-sided ECG featured only ST segment depression and inverted T-waves.

I Think Your Segments are Upside Down - Posterior 12-Lead

Reviewing the posterior leads, we see some interesting changes. Notably ST segment elevation of 0.5 mm in V7 and V8, and an unchanged appearance of the limb leads.

So, Dr. Walsh, what can we take away from this case?

Devoted readers of EMS 12-Lead will already know much about posterior MI, so I'll just do a brief review of the basics. I encourage you to search for the tag "posterior STEMI" for more information. As always, Dr. Stephen Smith's website also has plenty of examples and teaching about posterior MIs.

There is a small amount of controversy about what anatomic area of the heart a "posterior" MI actually affects. Some have suggested that the infarct is actually in the infero-basal region, while others have evidence that it should be viewed as a lateral infarct.

Inferiobasal versus Lateral

Regardless of the name, however, it generally is the result of an occlusion of the left circumflex coronary artery (link to cool animation). This territory is generally regarded as "electrically silent" in the standard ECG leads. As such, diagnosis relies on indirect evidence in the standard leads, as well as the use of non-standard "posterior" ECG leads.

So, how can we be Posterior STEMI Rock Stars, Doc?

For years, the standard teaching on identifying a posterior MI has emphasized some common elements. Brady summarized the most important of these:

  • Horizontal ST depression in V1-V4
  • Tall, broad R waves (>30ms)
  • Upright T waves
  • Dominant R wave (R/S ratio > 1) in V2

So, a typical posterior STEMI looks like this:

Posterior STEMI - Courtesy of LifeInTheFastLane.com

Inferioposterior STEMI courtesy of LifeInTheFastLane.

Note the ST elevations in the inferior and lateral leads; in general, a posterior MI usually shows signs of a STEMI in either of these two regions the majority of the time. It's pretty obvious that evidence of STEMI in one area (e.g. inferior) certainly strengthens suspicion for a posterior MI. 

However, here's an example of a posterior MI that does not show any inferior or lateral involvement:

Posterior STEMI without Inferiolateral Changes

Posterior STEMI without inferiolateral changes. (PubMed)

Using posterior leads (V7-V9) can show ST elevation, but the magnitude may not be as dramatic as that seen in the "usual" STEMIs. Many experts consider, for example, 0.5 mm of elevation to be significant, instead of the usual > 1 mm criteria, and that elevation in just one lead is sufficient.

So what's wrong with the conventional thinking?

There's a short-cut way to diagnose a posterior MI, that involves "flipping" the ECG. The idea is that the ST depression in the anterior leads is a "mirror" view of ST elevation in the posterior wall, and that the tall R-waves are actually deep Q-waves.

For example,  a blow-up of lead V2 from the isolated posterior MI above (the second ECG) looks like this:

Initial ECG - V2

It fulfills all the criteria I reviewed above, so it's a classic example of how we currently define a posterior MI. And if we "flip" it, we get this:

Initial ECG - V2 Flipped

Yep Doc, that looks like a regular STEMI now!

For many people (MDs included!), the diagnosis of a posterior MI starts, and ends, with this flipping.

I'll tell you what has always bothered me though. Look at the R-wave in the un-flipped image. This is just the mirror image of the Q-wave, and our "flipped" image reinforces that. In fact, the Q-wave in our flipped image looks pretty darn old, like the MI has progressed far along already. 

Furthermore, the T-wave in our "flipped" image hardly looks hyper-acute. In fact, it looks like the T-waves are in the process of returning to baseline, another indication that our "classic" posterior MI is old. 

Here's an example of an subacute/old inferior MI, for comparison. Also note the resolving, partially inverted, T-waves in III and aVF:

Old Inferior MI - Courtesy of LifeInTheFastLane

Old Inferior MI courtesy of LifeInTheFastLane.

It looks instead like our description of posterior MI is training us to look for old, completed MIs! 

Let's look at this from another angle. Look at this typical inferior STEMI, and focus on lead aVF:

Typical Inferior MI courtesy of LifeInTheFastLane

That's a classic STEMI, no doubt. Tiny Q-waves, tall T-wave – everything suggests that this is very acute.

Now, instead of being lead aVF, let's pretend it were lead V9. What would the "flipped" view of this lead be? Let's flip it and see!

Typical MI - aVF Flipped (V9 Equivalent)

This view shows a small R-wave, and a fully inverted and deep T-wave. Now, if we take a look back at the criteria listed above for a posterior MI, however, it would not meet much of the description of a posterior MI we listed before.

We're teaching people to pick up on old posterior MIs, and training them to miss the acute presentations.

Interesting, so how can we avoid this, Doc?

Well, I may have had this thought kicking around in my head, but some cardiologists actually wrote down these thoughts! Birnbaum et al. just published the article Common pitfalls in the interpretation of electrocardiograms from patients with acute coronary syndromes with narrow QRS: a consensus report. This wasn't a prospective controlled trial, but they managed to get 13 cardiologists to agree on a few things. 

One of those was that our standard description of the morphology of posterior MI on the ECG is likely wrong. Helpfully, they proceed to describe what we ought to be looking for!

After reviewing the usual evolution of LCx-occlusion MI, they conclude that the standard definition, that relies on tall R-waves and upright T-waves is: 

… the late “mirror image” of fully evolved ST-segment MI (STEMI) (Q waves with terminal T-wave inversion) and not the acute phase of STEMI. 

By contrast, they give an example of what they consider to be an acute posterior STEMI:

Birnbaum - Typical Acute Posterior STEMI

If we blow up lead V2…

Birnbaum - V2 Blowup

…we see that there is a small R-wave, and fully inverted T-waves, and an R/S < 1. It meets none of Brady's criteria above. But if we flip it…

Birnbaum - V2 Blownup and Flipped

It looks like a regular ol' STEMI!

Bring it home for us, doc.

The usual description of posterior MI may be in need of revision. The posterior leads, however, remain useful to reveal acute cardiac ischemia.

Thank you again to Dr. Brooks Walsh for this case and his insight into posterior STEMI!

  • Did you catch the posterior STEMI?
  • Does your service allow you to activate a posterior STEMI?
Posted by on November 2, 2012 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , ,

63 year old male CC: Substernal Chest Pain

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Today we're presenting a case from our friend Dr. Brooks Walsh of Mill Hill Avenue Command and Doc Cottle's Desk. In fact, this case is being presented both for his readers and for ours! We hope you like it.

You're working ED triage when a 63-year-old man walks in complaining of substernal chest pressure that had awoken him from sleep 2 hours prior. He denied any radiation of the pain, but complained of some mild presyncopal symptoms. His wife reported that he had had intense diaphoresis at home. He reported having a similar episode 1 year ago, but a subsequent stress test was negative. 

You obtain a quick history:

  • PMHx: HTN, type 2 diabetes mellitus
  • Meds: irbesartan, insulin
  • Allergies: NKDA 

A quick set of vitals are obtained:

  • HR: 90 
  • BP: 145/123 (NIBP)
  • RR: 16, unlabored
  • SaO2: 98% r/a

The physical exam reveals a patient with mild sweating, but no JVD. His lungs are clear, there are no cardiac murmurs, and he does not have any lower extremity swelling or tenderness.

You obtain a STAT 12-Lead ECG:

I Think Your Segments are Upside Down - Initial 12-Lead

The patient is taken back to a bed, 324mg of aspirin is administered, an IV is started, and labs are drawn. The patient receives 0.4 mg SL nitroglycerin and 5 mg morphine, both without relief. Metoprolol is given for the patient's hypertension and a heparin drip initiated. Cardiology was consulted and believed the ECG to be non-specific. 

Per the ED physician, an ECG is performed 15 minutes later to assess the right side of the heart. Note that all of the precordial leads were reversed (e.g. V2R = V1):

I Think Your Segments are Upside Down - Right-Sided 12-Lead

Due to persistent chest pain, a nitroglycerin drip is initiated and titrated up to 132 mcg/min without improvement in chest pain. A loading dose of clopidogrel is given.

An hour after presentation the ED physician asks for a posterior ECG:

I Think Your Segments are Upside Down - Posterior 12-Lead

Labs return a troponin of 0.05 (normal is < 0.04). A CBC and basic chemistry panel were essentially negative.

 

  • What does the first ECG show? Is it diagnostic?
  • Do the right-side and posterior leads help with diagnosis? 
  • If this is a STEMI, what coronary artery is likely involved? 
Posted by on October 29, 2012 • Filed under: ems-topics, patient-management • Tagged: , , , , ,

Episode #10 – Brooks Walsh, M.D. from Mill Hill Ave Command

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EMS 12-Lead podcast – Episode #10 – Brooks Walsh, M.D. from the Mill Hill Ave Command blog 

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In this episode of the EMS 12-Lead podcast we're joined by Brooks Walsh, M.D., Emergency Physician and Editor of Mill Hill Ave Command and Doc Cottle's Desk. We discuss paramedic education, ECGs, blogging, science fiction doctors, "treating the patient and not the monitor", reperfusion therapy for acute STEMI, and preactivation of the cardiac cath lab.

Brooks Walsh, M.D.

See also:

Mill Hill Ave Command

Dr. Cottle's Desk

Follow Brooks Walsh, M.D. on Twitter: @BrooksWalsh

Follow the Mill Hill Ave Command blog on Facebook

Subscribe to the EMS 12-Lead podcast on iTunes

Posted by on October 7, 2012 • Filed under: ems-topics, patient-management • Tagged: , , , ,